期刊
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
卷 309, 期 3, 页码 E283-E292出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00043.2015
关键词
humanin; triglyceride secretion; hepatic microsomal triglyceride transfer protein; hypothalamus
资金
- Department of Pediatrics of the University of Pittsburgh School of Medicine
- National Institutes of Health [K08-AG-027462, K08-AG-027462-03S1, R01-AG-035114]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK098437] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [K08AG027462, R01AG035114] Funding Source: NIH RePORTER
Humanin (HN) is an endogenous mitochondria-associated peptide that has been shown to protect against various Alzheimer's disease-associated insults, myocardial ischemia-reperfusion injury, and reactive oxygen species-induced cell death. We have shown previously that HN improves whole body glucose homeostasis by improving insulin sensitivity and increasing glucose-stimulated insulin secretion (GSIS) from the beta-cells. Here, we report that intraperitoneal treatment with one of HN analogs, HNG, decreases body weight gain, visceral fat, and hepatic triglyceride (TG) accumulation in high-fat diet-fed mice. The decrease in hepatic TG accumulation is due to increased activity of hepatic microsomal triglyceride transfer protein (MTTP) and increased hepatic TG secretion. Both intravenous (iv) and intra-cerebroventricular (icv) infusion of HNG acutely increase TG secretion from the liver. Vagotomy blocks the effect on both iv and icv HNG on TG secretion, suggesting that the effects of HNG on hepatic TG flux are centrally mediated. Our data suggest that HN is a new player in central regulation of peripheral lipid metabolism.
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